Cold Spring Harbor Perspectives in Biology· 2012Q1· Preprint
NMDA Receptor-Dependent Long-Term Potentiation and Long-Term Depression (LTP/LTD)
- 1,105citations
- Q1SCImago
- 2012year
Short summary
NMDA receptor activation triggers synaptic strengthening (LTP) or weakening (LTD) via AMPA receptor redistribution and, over time, structural changes requiring new protein synthesis.
AI-generated from the title and abstract; the full text is not read.
Key points
- NMDA receptor activation is a key trigger for both LTP and LTD.
- Early synaptic plasticity involves AMPA receptor redistribution.
- Long-term plasticity requires structural changes and new protein synthesis.
- NMDA receptor-dependent LTP/LTD are considered cellular substrates for learning and memory.
AI-generated from the title and abstract; the full text is not read.
Abstract
Long-term potentiation and long-term depression (LTP/LTD) can be elicited by activating N-methyl-d-aspartate (NMDA)-type glutamate receptors, typically by the coincident activity of pre- and postsynaptic neurons. The early phases of expression are mediated by a redistribution of AMPA-type glutamate receptors: More receptors are added to potentiate the synapse or receptors are removed to weaken synapses. With time, structural changes become apparent, which in general require the synthesis of new proteins. The investigation of the molecular and cellular mechanisms underlying these forms of synaptic plasticity has received much attention, because NMDA receptor-dependent LTP and LTD may constitute cellular substrates of learning and memory.
The authors' abstract, as published at the source. Cold Spring Harbor Perspectives in Biology, 2012 · DOI ↗
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Field: Cellular and Molecular Neuroscience
Cellular and Molecular NeuroscienceNeuroscience